Tissue-intrinsic beta-catenin signals antagonize Nodal-driven anterior visceral endoderm differentiation

Sina Schumacher, Max Fernkorn, Michelle Marten, Rui Chen, Yung Su Kim, Ivan Bedzhov and Christian Schröter ()
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Sina Schumacher: Max Planck Institute of Molecular Physiology
Max Fernkorn: Max Planck Institute of Molecular Physiology
Michelle Marten: Max Planck Institute of Molecular Physiology
Rui Chen: Max Planck Institute for Molecular Biomedicine
Yung Su Kim: Max Planck Institute for Molecular Biomedicine
Ivan Bedzhov: Max Planck Institute for Molecular Biomedicine
Christian Schröter: Max Planck Institute of Molecular Physiology

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract The anterior-posterior axis of the mammalian embryo is laid down by the anterior visceral endoderm (AVE), an extraembryonic signaling center that is specified within the visceral endoderm. Current models posit that AVE differentiation is promoted globally by epiblast-derived Nodal signals, and spatially restricted by a BMP gradient established by the extraembryonic ectoderm. Here, we report spatially restricted AVE differentiation in bilayered embryo-like aggregates made from mouse embryonic stem cells that lack an extraembryonic ectoderm. Notably, clusters of AVE cells also form in pure visceral endoderm cultures upon activation of Nodal signaling, indicating that tissue-intrinsic factors can restrict AVE differentiation. We identify β-catenin activity as a tissue-intrinsic factor that antagonizes AVE-inducing Nodal signals. Together, our results show how an AVE-like population can arise through interactions between epiblast and visceral endoderm alone. This mechanism may be a flexible solution for axis patterning in a wide range of embryo geometries, and provide robustness to axis patterning when coupled with signal gradients.

Date: 2024
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DOI: 10.1038/s41467-024-49380-0

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